Medical science monitor : international medical journal of experimental and clinical research · 2011
Association of clinical and aetiologic subtype of acute ischaemic stroke with inflammation, oxidative stress and vascular function: a cross-sectional observational study.
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Beer Christopher, Blacker David, Hankey Graeme J, Puddey Ian B
Аннотация
BACKGROUND: The role of inflammation, vascular dysfunction and oxidative stress in the pathophysiology of different stroke subtypes is not well understood. We aimed to determine if the clinical and aetiologic subtype of acute ischaemic stroke influences systemic markers of vascular function, inflammation and oxidative stress.
MATERIAL/METHODS: 129 men and women were recruited within 10 days of acute ischaemic stroke or TIA at two tertiary hospitals in this cross-sectional observational study. Stroke severity (NIHSS score and S100B concentration); systemic markers of inflammation (high sensitivity C-reactive protein [hs-CRP] and fibrinogen), endothelial activation (E-selectin), endothelial cell damage (von Willebrand factor activity), and oxidative stress (F2-isoprostanes) were measured.
RESULTS: Hs-CRP concentrations were higher in total anterior (22.0 ± 24.1 mg/L) than partial anterior circulation (15.3 ± 32.4 mg/L) and lacunar (4.9 ± 4.3 mg/L) syndromes (p = 0.01). Hs-CRP concentrations correlated moderately with NIHSS score (r = 0.45, p < 0.01) and S100B (r = 0.48, p < 0.01). However aetiologic and clinical subtypes were not independently associated with hs-CRP when included with stroke severity in general linear models.
CONCLUSIONS: These data suggest that stroke aetiology and clinical syndrome may not be important independent determinants of the degree of systemic inflammation, oxidative stress or endothelial function in acute ischaemic stroke. Other factors, including stroke severity, pre-morbid inflammation and co-morbidity may explain variations among groups of participants with different subtypes of acute ischaemic stroke.
MATERIAL/METHODS: 129 men and women were recruited within 10 days of acute ischaemic stroke or TIA at two tertiary hospitals in this cross-sectional observational study. Stroke severity (NIHSS score and S100B concentration); systemic markers of inflammation (high sensitivity C-reactive protein [hs-CRP] and fibrinogen), endothelial activation (E-selectin), endothelial cell damage (von Willebrand factor activity), and oxidative stress (F2-isoprostanes) were measured.
RESULTS: Hs-CRP concentrations were higher in total anterior (22.0 ± 24.1 mg/L) than partial anterior circulation (15.3 ± 32.4 mg/L) and lacunar (4.9 ± 4.3 mg/L) syndromes (p = 0.01). Hs-CRP concentrations correlated moderately with NIHSS score (r = 0.45, p < 0.01) and S100B (r = 0.48, p < 0.01). However aetiologic and clinical subtypes were not independently associated with hs-CRP when included with stroke severity in general linear models.
CONCLUSIONS: These data suggest that stroke aetiology and clinical syndrome may not be important independent determinants of the degree of systemic inflammation, oxidative stress or endothelial function in acute ischaemic stroke. Other factors, including stroke severity, pre-morbid inflammation and co-morbidity may explain variations among groups of participants with different subtypes of acute ischaemic stroke.